The importance of the aorta as a source of emboli has only recently become apparent since the advent of transesophageal echocardiography (TEE). This technique has enabled physicians to visualize the aortic wall in great detail and to quantify atheromatous aortic plaque according to thickness, degree of intraluminal protrusion, and presence or absence of mobile components. See Katz et al., Journal of the American College of Cardiology 20: 70-77 (1992), this and all other references cited herein are expressly incorporated by reference as if set forth herein in their entirety. Anecdotal reports linking embolic events to the presence of mobile aortic atheroma have lead to large-scale studies aimed at establishing the exact relationship between aortic atheromatosis and cerebral embolization. See Flory, American Journal of Pathology 21:549-565 (1945); Beal et al., Neurology 31:860-865 (1981); Soloway et al., Archives of Neurology 11:657-667 (1973); Russell et al., Stroke 22:253-258 (1991); and Tunick et al., Annals of Internal Medicine 114:391-392 (1991).
In 1992, and again in 1994, Amarenco disclosed an unequivocal association between embolic stroke and TEE-detected aortic plaque, especially in the presence of mobile plaque. See Amarenco et al., Stroke 23:1005-1009 (1992); and Amarenco et al., New England Journal of Medicine 331:1474-1479 (1994). Amarenco performed a prospective, case-control study of the frequency and thickness of atherosclerotic plaques in the ascending aorta and proximal arch in 250 patients with stroke and in 250 controls. Amarenco found protruding plaque (4 mm) in 14.4% of patients with stroke but only 2% of control. Plaques of all thickness were associated with stroke, but the association was strongest for plaques more than 4 mm in thickness. Protruding plaque was present in 28.2% of 78 patients with stroke of unknown cause, compared with 8.1% of 172 patients with stroke of known or likely causes. Furthermore, mobile plaque was present in 7.7% of patients with stroke of unknown cause, compared with only 0.6% of patients with stroke of known cause. The association between protruding atheroma and stroke was strongest for ascending aorta and proximal arch, but weaker for the distal arch and descending aortic disease.
Ulcerated aortic plaque, the pathologic correlate of TEE-detected mobile plaque, was present in autopsies of 26% of 239 patients with cerebrovascular disease as compared with 5% of 261 patients with other neurologic diseases. The prevalence of ulcerated arch lesions was 61% among 28 patients with no known causes of brain infarction, as compared with 22% among 155 patients with a known cause of infarction. See Amarenco et al., New England Journal of Medicine 326:221-225 (1992).
Amarenco and others showed prospectively (following patients for two years) a strong correlation between mobile plaque and embolic stroke or emboli to the legs and/or kidneys. In an attempt to investigate the value of aortic atheroma in predicting future vascular events, Tunick followed 42 patients with TEE-detected protruding atheroma and an equal number of controls for up to two years. See Tunick et al., Journal of the American College of Cardiology 23:1085-1090 (1994). Fourteen (33%) patients with protruding plaque had 19 embolic events, as compared with 3 out of 42 (7%) controls. These observations have been independently confirmed by a number of other recent studies on risk factors of embolic stroke. See Tunick et al., American Heart Journal 120:658-660 (1990), Karalis et al., Journal of the American College of Cardiology 17:73-78 (1991), Tunick et al., Annals of Internal Medicine 115:423-427 (1991), Tunick et al., American Heart Journal 124:239-241 (1992), Horowitz et al., Neurology 42:1602-1604 (1992), Toyoda et al., Stroke 23:1056-1061 (1992), Nihoyannopoulos et al., American Journal of Cardiology 71:1208-1212 (1993), Davila-Roman et al., Stroke 25:2010-2016 (1994), and the French Study of Aortic Plaques in Stroke Group, New England Journal of Medicine 334(19):1216-1221 (1996).
The danger of embolic stroke from atheroma present in the aorta, especially of mobile plaque, has been shown in patients undergoing cardiac surgery, and this effect is due to mechanical manipulations performed on the aorta during cardiac surgery. See Hartman, et al., Anesthesia Analgesia 1996 (in press), Gold et al., Journal of Thoracic Cardiovascular Surgery 110:1302-1314 (1995), Marshall et al., Annals of Thoracic Surgery 48:339-344 (1989), Katz et al., Journal of American College of Cardiology 20:70-77 (1992); and Hosoda et al., Journal of Cardiovascular Surgery 32:301-306 (1991). In fact, among patients undergoing coronary bypass surgery, aortic atheromatosis has emerged as the single most important factor in perioperative neurologic morbidity. See Tunick et al., Annals of Internal Medicine 114:391-392 (1991); Karalis et al., Journal of the American College of Cardiology 17:73-78 (1991); Marschall et al., Journal of Cardiothoracic Vascular Anesthesia 8:5-13 (1994); Blauth et al., Journal of Thoracic Cardiovascular Surgery 103:1104-1112 (1992); Wareing et al., Journal of Thoracic Cardiovascular Surgery 103:453-462 (1992); Ribakove et al., Annals of Thoracic Surgery 53:758-763 (1992); Brillman, Neurologic Clinics 11:475-495 (1993); and Amarenco et al., Stroke 23:1005-1009 (1992). As the number of elderly patients undergoing bypass surgery has increased, the decline in overall mortality and cardiac morbidity achieved by improvements in surgical and anesthetic techniques has been largely obscured by increasing neurologic complication rates. See Loop et al., Cleveland Clinical Journal of Medicine 55:23-24 (1988); Hill et al., Annals of Thoracic Surgery 7:409-419 (1969); Gardner et al., Annals of Thoracic Surgery 40:574-581 (1985); and Cosgrove et al., Journal of Thoracic Cardiovascular Surgery 88:673-684 (1984). Aortic atheroma increases sharply with age, from 20% in the fifth decade at necropsy to 80% over the age of 75 years, and stroke rate increases from 1% in patients 51 to 60 years to 7% or more in those over 75 years. See Fisher et al., Journal of Neuropathology and Experimental Neurology 24:455-476 (1965); Amarenco et al., Stroke 23:1005-1009 (1992); Marschall et al., Journal of Cardiothoracic Vascular Anesthesia 8:5-13 (1994); Blauth et al., Journal of Thoracic Cardiovascular Surgery 103:1104-1112 (1992); Wareing et al., Annals of Thoracic Surgery 55:1400-1408 (1993); and Davila-Roman et al., Circulation 84 III-47-III-53, 1991; Wareing et al., Journal of Thoracic Cardiovascular Surgery 103:453-462 (1992); Gardner et al., Annals of Thoracic Surgery 40:574-581 (1985); Cosgrove et al., Journal of Thoracic Cardiovascular Surgery 88:673-684 (1984); Davila-Roman et al., Stroke 25:2010-2016 (1994); Bar-El et al., Journal of Thoracic Cardiovascular Surgery 104:469-474 (1992); and Saloman et al., Journal of Thoracic Cardiovascular Surgery 101:209-218 (1991). Among patients dying after coronary bypass surgery, evidence of atheroembolism was present in only 4.5% in 1982, and in as many as 48% in 1989. See Wareing et al., Journal of Thoracic Cardiovascular Surgery 103:453-462 (1992).
Embolization from the aorta, particularly to the brain, is therefore a major problem, and emboli from this source can lead to stroke, myocardial infarction, kidney infarcts, and peripheral emboli in other organs. There is a presently unfulfilled need for an atherectomy device for use in the aorta to prevent the above identified disorders arising from embolization. Moreover, it will be understood that fixed plaque exists both in the aorta and in the carotid arteries which may also lead to stroke by embolization. Thus, there is a presently unfulfilled need for an atherectomy device for use in both aorta and carotid arteries to prevent embolization from such fixed plaque. Another site at which fixed plaque may build up is in the iliac and femoral arteries. Claudication may result from inadequate blood flow in or embolization to the iliac and femoral arteries. A need therefore exists for an atherectomy device for use in the iliac and femoral arteries to prevent claudication by increasing blood flow and also preventing embolization to the lower extremities.
The coronary arteries, by contrast, present entirely different considerations with respect to atherectomy. In the coronary arteries, myocardial ischemia or infarction is typically caused by a reduction in blood flow by reason of the build up of atheroma causing stenosis, rather than dislodgement of embolic material from such plaques. Atherectomy in the coronary arteries therefore prevents myocardial infarction by increasing blood flow due to an enlargement of the luminal diameter on removal of stenosis. Accordingly, there exists an extensive body of literature which addresses the use of atherectomy in relation to stenosis as applied in the coronary arteries. For example, Fischell, U.S. Pat. No. 5,409,454, discloses a retrograde cutting atherectomy catheter designed to perform atherectomy on an eccentric stenosis by cutting plaque from one part of an arterial wall while shielding a normal portion of the arterial wall from being cut. Fischell, U.S. Pat. No. 4,898,575, discloses a tunneling catheter system which rides on a guidewire for percutaneous transluminal atherectomy. Rydell, U.S. Pat. No. 4,857,045, discloses an atherectomy catheter having a motor driven cutting member and capabilities for flushing the treatment site and aspirating a flushing liquid so as to remove debris loosened during a procedure. Moreover, Yock, U.S. Pat. Nos. 4,794,931, 5,000,185, and 5,313,949, disclose catheters having a cutting member for atherectomy and an ultrasound transducer which enables ultrasonography in combination with atherectomy. Meanwhile, Jang et al., U.S. Pat. No. 5,507,292, discusses abrasive atherectomy in combination with ultrasound imaging. The patent and medical literature is replete with additional disclosures of atherectomy as applied to the coronary arteries, and this subject will not be further discussed here for the sake of brevity. The interested reader is referred to the following disclosures for more information: Farr, U.S. Pat. Nos. 4,950,277, 4,986,807, 5,019,088, Shiber, U.S. Pat. Nos. 4,894,051, 4,957,482, 4,979,939, 5,007,896, 5,024,651, 5,135,531, Summers, U.S. Pat. No. 5,087,265, Plassche et al., U.S. Pat. No. 5,318,576, Belknap, U.S. Pat. No. 5,366,464, Jang et al., U.S. Pat. No. 5,402,790, Mazur et al., Catherization and Cardiovascular Diagnosis 31:79-84 (1994), Fischell et al., U.S. Pat. Nos. 4,886,061, 5,100,425. It will be appreciated that coronary artery atherectomy devices do not prevent embolization, but this does not appear to be a major consequence during this procedure.
Insofar as we are aware, however, there has been no disclosure of an atherectomy catheter adapted for trapping and removing mobile plaque or fixed plaque in the aorta, carotid, or femoral arteries and having an ability to remove embolic material generated during the procedure. Accordingly, a need exists for an arterial atherectomy catheter having an ability to entrap and/or snare, and thereafter remove aortic, carotid, and femoral artery plaque without generating atheromatous embolization.